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We transplanted F344 rat hepatocytes into syngeneic dipeptidyl peptidase IV-deficient F344 rats. Changes in cyclooxygenase pathways were analyzed, and specific pathways were blocked pharmacologically; the effects on cell engraftment and native liver cells were determined.
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Osteoarthritis is increasingly recognized as a complex illness in which interrelationships between the different tissues of the joint are important. We are still some way from a complete understanding of the pathophysiologic and temporal relationships between bone, synovial tissue and cartilage. Recent evidence points to a significant role for cytokines and growth factors in osteoarthritis that leads to a preponderance of catabolic processes in the joint. In-vitro culture of human cartilage has been used as a model to measure the effects of drugs used in the treatment of osteoarthritis on anabolic and catabolic processes. On this basis, the nonsteroidal antiinflammatory drugs can be categorized into one of three classes depending on whether they are inhibitory (e.g., indomethacin and naproxen), neutral (e.g., diclofenac, aspirin and piroxicam) or stimulatory (e.g., aceclofenac, tenidap and tolmetin) of glycosaminoglycan synthesis in chondrocytes. The marked differences between these nonsteroidal antiinflammatory drugs suggest that a mechanism other than cyclooxygenase inhibition is involved in their effects on glycosaminoglycan synthesis. Inhibition of IL-1beta and the stimulation of growth factors are suggested as possible mechanisms. Although the significance of these properties of nonsteroidal antiinflammatory drugs awaits confirmation in in-vivo and clinical situations, they do provide the clinician with a new parameter with which to choose therapy in osteoarthritis.
Forty endoscopically normal healthy subjects were randomized to receive either BID salsalate (3500 mg/day) or BID naproxen (750 mg/day) for 14 days followed by repeat endoscopic examination. Gastroduodenal lesions were found in 55% (11/20) of the subjects taking naproxen, and 10% (2/20) of those taking salsalate (p = 0.002). Twenty-five percent (5/20) of the subjects taking naproxen and none of the subjects taking salsalate were noted to have severe gastric injury (p = 0.003). There was no difference between the 2 groups in subjective gastrointestinal system adverse experiences. Overall, 95% (19/20) of subjects taking salsalate reported at least 1 adverse experience compared with 60% (12/20) of those taking naproxen (p = 0.02). This was due primarily to the higher number of subjects taking salsalate reporting reversible tinnitus or hearing loss. There was no significant treatment difference in adverse experiences reported for any other organ system. The results of our study support previous observations in patients with rheumatoid arthritis that salsalate produces less gastroduodenal mucosal toxicity than the widely used antiinflammatory agent, naproxen.
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The occurrence, behavior, and release of five acidic pharmaceuticals, including ibuprofen (IBP), naproxen (NPX), ketoprofen (KEP), diclofenac (DFC), and clofibric acid (CA), have been investigated along the different units in a tertiary-level domestic wastewater treatment plant (WWTP) in hyper-urbanization city of China (Shanghai). IBP was the most abundant chemicals among the measured in raw wastewater. The loads of the acidic pharmaceuticals in the WWTP influent ranged from 7.5 to 414 mg/day/1,000 inh, which were lower than those reported in the developed countries suggesting a less per capita consumption of pharmaceuticals in Shanghai. IBP obtained by highest removal (87 %); NPX and KEP were also significantly removed (69-76 %). However, DFC and CA were only moderately removed by 37-53 %, respectively. Biodegradation seemed to play a key role in the elimination of the studied pharmaceuticals except for DFC and CA. An annual release of acidic pharmaceuticals was estimated at 1,499 and 61.7 kg/year through wastewater and sludge, respectively, from Shanghai. Highest pharmaceuticals concentrations were detected in the effluent discharge point of the WWTP, indicating that WWTP effluent is the main source of the acidic pharmaceuticals to its receiving river. Preliminary results indicated that only DFC in river had a high risk to aquatic organisms. Nevertheless, the joint toxicity effects of these chemicals are needed to further investigate.
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) in children has rapidly escalated over the last 5 years in Australia. This is primarily as a result of the availability of ibuprofen as an over-the-counter preparation. Several recent, significant adverse drug reactions (ADRs) to NSAIDs, at the Royal Children's Hospital (RCH) in Melbourne, Australia prompted review of all of the RCH reactions reported to these agents over 5 years.
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1. Rat liver microsomal suspension containing NADPH and MgCl2 was incubated at 37 degrees C with naproxen, a non-steroidal anti-inflammatory drug. Thiobarbituric acid reactive substances (TBA-RS), high molecular weight protein aggregates and fluorescent substances were formed in the microsomal suspension. 2. Chemiluminescence was produced from the microsomal suspension. This chemiluminescence production was well correlated to the TBA-RS formation, indicating that the chemiluminescence production was closely associated with the lipid peroxidation. 3. The addition of SKF-525A to the microsomal suspension inhibited the production of TBA-RS, chemiluminescence and 6-demethylnaproxen (6-DMN), the oxidative product of naproxen. Further, the antioxidant, alpha-tocopherol and singlet oxygen quenchers like histidine, dimethylfuran and 1,4-diazabicyclo[2,2,2]octane strikingly inhibited the productions of chemiluminescence and TBA-RS. 4. Neither naproxen nor 6-DMN caused lipid peroxidation in the absence of NADPH. Thus, lipid peroxidation and chemiluminescence during the oxidation of naproxen in liver microsomes was suggested to be provoked by reactive oxygen species and an origin of chemiluminescence was shown to be singlet oxygen.
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To reassess the prevalence of aspirin induced asthma and other issues related to the syndrome.
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A case-control study was performed with prospective recruitment of cases of gastrointestinal bleeding or ulcer perforation and age- and sex-matched controls. Information on preadmission drug use obtained by structured interview.
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Lateral epicondylitis is a painful condition responsible for loss of function and sick leave for long periods of time. In many countries, the treatment guidelines recommend a wait-and-see policy, reflecting that no conclusions on the best treatment can be drawn from the available research, published studies and meta-analyses.
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Male Wistar rats were equipped with an exteriorized canula in the proximal jejunum. LPS or vehicle were administered into the jejunum (10 mg ml(-1)). For further study of molecular mechanisms, LPS or vehicle were administered systemically (1 mg kg(-1)). Brain stem activation was quantified by Fos-immunohistochemistry in the vagal nucleus of the solitary tract (NTS) and the Area postrema which is exposed to systemic circulation. Serum LPS concentrations were also determined.
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HCP1004 is a newly developed fixed-dose combination of naproxen (500 mg) and esomeprazole strontium (20 mg) that is used in the treatment of rheumatic diseases and can reduce the risk of nonsteroidal anti-inflammatory drug-associated ulcers. The aim of this study was to evaluate the pharmacokinetics (PK) and safety of HCP1004 compared to VIMOVO(®) (a marketed fixed-dose combination of naproxen and esomeprazole magnesium).
Several lines of evidence indicate that abscisic acid (ABA) is derived from 9'-cis-neoxanthin or 9'-cis-violaxanthin with xanthoxin as an intermediate. (18)O-labeling experiments show incorporation primarily into the side chain carboxyl group of ABA, suggesting that oxidative cleavage occurs at the 11, 12 (11', 12') double bond of xanthophylls. Carbon monoxide, a strong inhibitor of heme-containing P-450 monooxygenases, did not inhibit ABA accumulation, suggesting that the oxygenase catalyzing the carotenoid cleavage step did not contain heme. This observation, plus the ability of lipoxygenase to make xanthoxin from violaxanthin, suggested that a lipoxygenase-like enzyme is involved in ABA biosynthesis. To test this idea, the ability of several soybean (Glycine max L.) lipoxygenase inhibitors (5,8,11-eicosatriynoic acid, 5,8,11,14-eicosatetraynoic acid, nordihydroguaiaretic acid, and naproxen) to inhibit stress-induced ABA accumulation in soybean cell culture and soybean seedlings was determined. All lipoxygenase inhibitors significantly inhibited ABA accumulation in response to stress. These results suggest that the in vivo oxidative cleavage reaction involved in ABA biosynthesis requires activity of a nonheme oxygenase having lipoxygenase-like properties.
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Incidence of GDUs was significantly lower in subjects receiving celecoxib plus aspirin (7%) compared with naproxen plus aspirin (25.3%; relative risk [RR], 0.28 [95% confidence interval (CI), 0.17-0.45]; P < 0.001), but significantly higher than placebo plus aspirin (1.6%; RR, 4.78 [95% CI, 1.12-20.32]; P = 0.016).
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To compare the efficacies of oral naproxen and oral tramadol for pain relief after cesarean delivery, and to evaluate administration at fixed intervals versus on request.
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Piroxicam is an N-heterocyclic carboxamide of 1,2 benzothiazine 1,1 dioxide with analgesic and anti-inflammatory activity. It has an extended half-life of about 40 hours and is suitable for once daily administration. Published studies indicate that piroxicam 20mg daily is comparable with aspirin 3 to 6g. indomethacin 75 to 150mg, phenylbutazone 400mg, naproxen 500mg, ibuprofen 1200 to 2400mg and diclofenac 75mg in rheumatoid arthritis. In osteoarthritis, piroxicam 20mg daily is comparable in efficacy with aspirin 2.6 to 3.9g, indomethacin 75mg, naproxen 500mg and fenbufen 600mg but is generally better tolerated than aspirin or indomethacin in patients with arthritic diseases. Piroxicam 20mg was at least as effective as indomethacin 75mg in a study in ankylosing spondylitis. As with other non-steroidal anti-inflammatory drugs gastrointestinal complaints are the most frequently reported side effects and their frequency and severity appears to be dose-related.
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The arylpropionic acid derivatives (APADs) ketoprofen and tiaprofenic acid can provoke photoallergic dermatitis. Possible cross-reactivity between APADs is of importance in patients using nonsteroidal anti-inflammatory drugs. Because of the similarities in chemical structures, we investigated patients with photoallergy to ketoprofen or tiaprofenic acid, in order to study cross-reactivity between APADs and a possible pattern of cross-reactivity between benzophenone-containing molecules, so as to determine the molecular basis of photoallergy to ketoprofen or tiaprofenic acid. 10 patients with photoallergy to topical ketoprofen, 2 with photoallergy to oral tiaprofenic acid, and 15 control subjects with no history of contact dermatitis from APADs, nor from benzophenone-containing molecules, were photopatch tested in triplicate with ketoprofen, tiaprofenic acid, other APADs (alminoprofen, fenoprofen, flurbiprofen, ibuprofen and naproxen), benzophenone-containing molecules (fenofibrate, oxybenzone, sulisobenzone), and unsubstituted benzophenone. 1 set was irradiated with UVA light, 1 with solar-simulated irradiation and 1 dark control. Tests were read at 2, 3 and 4 days. Patients reacted to both ketoprofen and tiaprofenic acid (12/12), fenofibrate (8/12), oxybenzone (3/12) and unsubstituted benzophenone (11/12), but not to other APADs, nor to sulisobenzone. Tests remained negative in control patients. Photoallergy is due to the benzophenone moiety of ketoprofen, or to the very similar thiophene-phenylketone of tiaprofenic acid, but not to their arylpropionic function. This induces cross-reactivity to fenofibrate and oxybenzone but not to APADs without a benzophenone moiety, which may therefore probably be used in such patients. Unsubstituted benzophenone should be added to standard phototesting series.
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Randomized, controlled trial.
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In a parallel, randomized, double-blind fashion, a total of 60 healthy subjects (age range, 20-44 years) received 2 single doses of 750 mg AZD3582, 1500 mg AZD3582, 50 mg rofecoxib, 500 mg naproxen, or placebo (n = 12 per group). The first dose was given after a 5-day normal-sodium diet (150 mmol/d), and the second was given after a consecutive 3-day low-sodium diet (10 mmol/d). Urinary sodium excretion during normal sodium intake and glomerular filtration rate (GFR) (assessed by iohexol clearance) during sodium depletion were the primary variables measured.
The use of oral medication in the treatment of chronic musculoskeletal pain in the elderly requires careful selection of drugs to control pain with consideration for both the physiological state and the presence of disease(s). Recent advances have improved the understanding of biomolecular mechanisms of chronic pain. These include the production of powerful pro-inflammatory cytokines by glial and microglial cells, which then lead to activation of major pain pathways from the periphery through the dorsal horn and supra-spinal pathways to the somatosensory and other higher cortical centres. This has allowed better recognition for intervention with anti-inflammatory agents to control cytokine production (e. g. prednisolone, triamcinolone and other brain-penetrating corticosteroids). Advances in understanding of chronic pain have lead to recognition of neuronal PX2 puringergic receptors as potential sites for drugs to control pain by more selective actions. Pain control in the elderly involves extensive use of analgesics, among them the non-steroidal anti-inflammatory drugs (NSAIDs), paracetamol (acetaminophen), and various narcotics. Each of these has its drawbacks, mostly related to potential toxicities. Attempts to reduce the serious gastro-intestinal (GI) adverse effects of the NSAIDs by the introduction of the highly selective COX-2 inhibitors (coxibs) have only had limited benefit in reducing these untoward actions. Moreover, the risks of serious cardiovascular (CV) and renal side-effects, though statistically infrequent, are none the less of major concern. Cardio-renal effects have been attributed to some (e. g. diclofenac), but not all (e. g. naproxen) conventional NSAIDs. Here we make recommendations for a selection of certain NSAIDs to be used for pain therapy in the elderly in consideration of their relative safety and pharmacokinetics. While newer formulations of narcotics have given some advance in pain control, the application of this group of drugs requires close supervision in the elderly, especially those with cognitive decline, since drug actions on the central and peripheral nervous systems (CNS, PNS) can result in significant adverse effects of these agents (e. g. constipation, drowsiness, respiratory and cardiovascular decline). Improvements in the safety and effectiveness of musculoskeletal pain therapy in the elderly can only be achieved by identification and frequent re evaluation of the cause of the chronic pain and the impact on the patient's general medical state.
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Emulsion-solvent evaporation is an established method to fabricate amorphous drug-loaded microparticles. In some cases, however, the encapsulated drug is present in its crystalline form, which can affect drug release and negatively impact on other characteristics of the final product. This work aimed to investigate the factors that are responsible for the formation (and inhibition) of drug crystals in modified-release microparticles. Five acidic drugs were encapsulated into Eudragit S or Eudragit L microparticles. Drug crystallinity was observed when indometacin and naproxen were encapsulated, while crystallization was not observed in the case of ketoprofen, salicylic acid, or paracetamol (acetaminophen). All drug-loaded microparticles had single glass transition temperature (T(g) ) intermediate between the T(g) of the drug and that of the polymer. The drop in T(g) in the case of the paracetamol-loaded particles was higher than predicted from the Gordon-Taylor equation, indicating that paracetamol was acting as a plasticizer in this system. After melt quenching in the presence of the Eudragit polymers, the crystallization of paracetamol was inhibited. The ratio of drug to polymer in the microparticles was the major determinant of drug crystallization, as was the solubility of the drug in the processing solvent. This work confirms that drug crystallization is a complex phenomenon, and that drug-polymer molecular interactions play a role in the inhibition of drug crystallization.
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In endodontic treatment, solutions of sodium hypochlorite are widely used as an irrigating agent. It is an effective solvent of both necrotic and vital tissues, which makes it toxic to the surrounding tissues. Complications are rarely reported. Nevertheless, the acute symptoms caused by the toxic reaction must not be underestimated. Causes, treatment, and prevention of complications of sodium hypochlorite use are discussed, and three case reports are presented.